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Mapping the effect of APOE epsilon4 on gray matter loss in Alzheimer's disease in vivo.
Neuroimage. 2009 May 01; 45(4):1090-8.N

Abstract

Previous studies suggest that in Alzheimer's disease (AD) the Apolipoprotein E (APOE) epsilon4 allele is associated with greater vulnerability of medial temporal lobe structures. However, less is known about its effect on the whole cortical mantle. Here we aimed to identify APOE-related patterns of cortical atrophy in AD using an advanced computational anatomy technique. We studied 15 AD patients carriers (epsilon4+, age: 72+/-10 SD years, MMSE: 20+/-3 SD) and 14 non-carriers (epsilon4-, age: 69+/-9, MMSE: 20+/-5) of the epsilon4 allele and compared them to 29 age-and-sex matched controls (age: 70+/-9, MMSE: 28+/-1). Each subject underwent a clinical evaluation, a neuropsychological battery, and high-resolution MRI. UCLA's cortical pattern matching technique was used to identify regions of local cortical atrophy. epsilon4+ and epsilon4- patients showed similar performance on neuropsychological tests (p>.05, t-test). Diffuse cortical atrophy was detected for both epsilon4+ (p=.0001, permutation test) and epsilon4- patients (p=.0001, permutation test) relative to controls, and overall gray matter loss was about 15% in each patients group. Differences in gray matter loss between carriers and non-carriers mapped to the temporal cortex and right occipital pole (20% greater loss in carriers) and to the posterior cingulate, left orbitofrontal and dorsal fronto-parietal cortex (5-15% greater loss in non-carriers). APOE effect in AD was not significant (p>.74, ANOVA), but a significant APOE by region (temporal vs fronto-parietal cortex) interaction was detected (p=.002, ANOVA), in both early and late-onset patients (p<.05, ANOVA). We conclude that the epsilon4 allele modulates disease phenotype in AD, being associated with a pattern of differential temporal and fronto-parietal vulnerability.

Authors+Show Affiliations

LENITEM Laboratory of Epidemiology, Neuroimaging and Telemedicine, IRCCS Centro San Giovanni di Dio - FBF, Brescia, Italy.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19349226

Citation

Pievani, M, et al. "Mapping the Effect of APOE Epsilon4 On Gray Matter Loss in Alzheimer's Disease in Vivo." NeuroImage, vol. 45, no. 4, 2009, pp. 1090-8.
Pievani M, Rasser PE, Galluzzi S, et al. Mapping the effect of APOE epsilon4 on gray matter loss in Alzheimer's disease in vivo. Neuroimage. 2009;45(4):1090-8.
Pievani, M., Rasser, P. E., Galluzzi, S., Benussi, L., Ghidoni, R., Sabattoli, F., Bonetti, M., Binetti, G., Thompson, P. M., & Frisoni, G. B. (2009). Mapping the effect of APOE epsilon4 on gray matter loss in Alzheimer's disease in vivo. NeuroImage, 45(4), 1090-8. https://doi.org/10.1016/j.neuroimage.2009.01.009
Pievani M, et al. Mapping the Effect of APOE Epsilon4 On Gray Matter Loss in Alzheimer's Disease in Vivo. Neuroimage. 2009 May 1;45(4):1090-8. PubMed PMID: 19349226.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mapping the effect of APOE epsilon4 on gray matter loss in Alzheimer's disease in vivo. AU - Pievani,M, AU - Rasser,P E, AU - Galluzzi,S, AU - Benussi,L, AU - Ghidoni,R, AU - Sabattoli,F, AU - Bonetti,M, AU - Binetti,G, AU - Thompson,P M, AU - Frisoni,G B, Y1 - 2009/01/21/ PY - 2008/10/08/received PY - 2008/12/12/revised PY - 2009/01/07/accepted PY - 2009/4/8/entrez PY - 2009/4/8/pubmed PY - 2009/6/17/medline SP - 1090 EP - 8 JF - NeuroImage JO - Neuroimage VL - 45 IS - 4 N2 - Previous studies suggest that in Alzheimer's disease (AD) the Apolipoprotein E (APOE) epsilon4 allele is associated with greater vulnerability of medial temporal lobe structures. However, less is known about its effect on the whole cortical mantle. Here we aimed to identify APOE-related patterns of cortical atrophy in AD using an advanced computational anatomy technique. We studied 15 AD patients carriers (epsilon4+, age: 72+/-10 SD years, MMSE: 20+/-3 SD) and 14 non-carriers (epsilon4-, age: 69+/-9, MMSE: 20+/-5) of the epsilon4 allele and compared them to 29 age-and-sex matched controls (age: 70+/-9, MMSE: 28+/-1). Each subject underwent a clinical evaluation, a neuropsychological battery, and high-resolution MRI. UCLA's cortical pattern matching technique was used to identify regions of local cortical atrophy. epsilon4+ and epsilon4- patients showed similar performance on neuropsychological tests (p>.05, t-test). Diffuse cortical atrophy was detected for both epsilon4+ (p=.0001, permutation test) and epsilon4- patients (p=.0001, permutation test) relative to controls, and overall gray matter loss was about 15% in each patients group. Differences in gray matter loss between carriers and non-carriers mapped to the temporal cortex and right occipital pole (20% greater loss in carriers) and to the posterior cingulate, left orbitofrontal and dorsal fronto-parietal cortex (5-15% greater loss in non-carriers). APOE effect in AD was not significant (p>.74, ANOVA), but a significant APOE by region (temporal vs fronto-parietal cortex) interaction was detected (p=.002, ANOVA), in both early and late-onset patients (p<.05, ANOVA). We conclude that the epsilon4 allele modulates disease phenotype in AD, being associated with a pattern of differential temporal and fronto-parietal vulnerability. SN - 1095-9572 UR - https://www.unboundmedicine.com/medline/citation/19349226/Mapping_the_effect_of_APOE_epsilon4_on_gray_matter_loss_in_Alzheimer's_disease_in_vivo_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1053-8119(09)00022-6 DB - PRIME DP - Unbound Medicine ER -